The endocannabinoid system is a lipid signaling network that regulates appetite, energy balance, and glucose homeostasis across the brain, gut, liver, adipose tissue, and pancreas. Through endocannabinoids like 2-AG and anandamide acting on CB1 and CB2 receptors, this system links feeding behavior to insulin sensitivity, adipokine signaling, and inflammatory tone.
My graduate research examined how cannabinoid signaling contributes to metabolic dysfunction in diet-induced obesity, with a focus on the gut-brain axis and the adipoinsular network connecting adipose tissue to pancreatic insulin secretion. By comparing isolated THC against whole cannabis extract, I identified compound-specific effects on body weight, glucose tolerance, and tissue-specific gene expression — work that helped explain a long-standing epidemiological paradox: chronic cannabis users tend to have lower rates of obesity and type 2 diabetes despite cannabis's appetite-stimulating effects.
This research demonstrates that cannabinoid compound composition and receptor context determine therapeutic outcome in metabolic disease, supporting a more targeted approach to cannabinoid-based interventions than "THC vs. no THC" — directly relevant to compound optimization and mechanism-of-action work in metabolic drug development.
Techniques:
Transgenic & diet-induced obese mouse models (chronic dosing paradigms)
UPLC-MS/MS lipidomics and endocannabinoid quantification
Glucose tolerance testing and metabolic phenotyping
Tissue-specific gene expression analysis (adipose, pancreas, gut)
Comparative pharmacology (isolated compound vs. whole extract study design)
